Kirihara T, Matsumoto-Miyai K, Nakamura Y, Sadayama T, Yoshida S, Shiosaka S
Division of Structural Cell Biology, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara 630-0101, Japan.
Br J Dermatol. 2003 Oct;149(4):700-6. doi: 10.1046/j.1365-2133.2003.05484.x.
Neuropsin (KLK8), a serine protease of the kallikrein family, is thought to be involved in the function of keratinocytes, i.e. migration, differentiation and desquamation. However, how neuropsin participates is still unknown.
To observe the epidermal function of serine protease in neuropsin-deficient mice.
We irradiated the skin of neuropsin-deficient mice with ultraviolet light to induce acute inflammation and compared the morphology with that of wild-type mice.
We observed a phenotypic change in the epidermis. An acute inflammatory dose of ultraviolet light induced a marked increase in neuropsin mRNA expression in the skin. The signal intensity of the mRNA expression was highest on day 2-3 after irradiation, when keratinocytes were aligned irregularly in the recovery period. Morphological comparison between neuropsin -/- and +/+ mice revealed that an irregular alignment of cells in the thickened epidermis was obvious on day 2 after irradiation in the wild-type mice, whereas it was prolonged for at least 2 days in the neuropsin-deficient mice. The stratum corneum of neuropsin-deficient mice was remarkably thicker than that of the wild-type mice at 5, 14 and 21 days after irradiation. The increase, as a response to this stimulus, in involucrin immunoreactivity, a marker for cell envelope assembly, was delayed in the mutant mice.
Thus, neuropsin might be involved early in the process of differentiation, such as in the assembly of the cell envelope, but not in migration and desquamation.
神经蛋白酶(KLK8)是激肽释放酶家族的一种丝氨酸蛋白酶,被认为参与角质形成细胞的功能,即迁移、分化和脱屑。然而,神经蛋白酶如何参与其中仍不清楚。
观察神经蛋白酶缺陷小鼠中丝氨酸蛋白酶的表皮功能。
我们用紫外线照射神经蛋白酶缺陷小鼠的皮肤以诱导急性炎症,并将其形态与野生型小鼠进行比较。
我们观察到表皮出现表型变化。急性炎症剂量的紫外线照射可诱导皮肤中神经蛋白酶mRNA表达显著增加。mRNA表达的信号强度在照射后第2 - 3天最高,此时角质形成细胞在恢复期排列不规则。神经蛋白酶-/-和+/+小鼠的形态学比较显示,野生型小鼠在照射后第2天增厚的表皮中细胞排列不规则明显,而在神经蛋白酶缺陷小鼠中这种情况至少延长了2天。照射后5天、14天和21天,神经蛋白酶缺陷小鼠的角质层明显比野生型小鼠厚。作为对这种刺激的反应,突变小鼠中作为细胞包膜组装标志物的内披蛋白免疫反应性的增加延迟。
因此,神经蛋白酶可能在分化过程的早期参与,如细胞包膜的组装,但不参与迁移和脱屑。